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Effect of oral and intravenous diltiazem on whole blood platelet aggregability
J Utoh1, J E Zajkowski-Brown, H Harasaki
1Department of Biomedical Engineering and Applied Therapeutics, Cleveland Clinic Foundation, Ohio.
Diltiazem, a calcium channel blocker, is known to suppress platelet function in vitro. However, its in vivo effects on platelets have been controversial. The effect of diltiazem on both human and calf platelets was studied using impedance whole-blood aggregometry. In vitro, platelet aggregation induced by ADP (5 microM) or collagen (1 micrograms/ml) was significantly suppressed by 0.1 to 1.0 mM (45 to 450 micrograms/ml) of diltiazem in both species. In calves weighting 70 to 90 kg, platelet aggregability did not change after the oral administration of 180 mg diltiazem. In this condition, diltiazem was not detected in plasma samples. Intravenous injection of 0.5 mg/kg diltiazem also did not significantly alter the aggregability, although the PR interval on the ECG elongated (40 msec, p < .05), mean arterial pressure dropped (14 mmHg, p < .05), and diltiazem was readily detected in plasma (199 ng/ml, 0.4 microM). In conclusion, platelet aggregability is not altered by a clinical dosage of diltiazem that is sufficient to induce hemodynamic changes with therapeutic plasma concentrations.
Diltiazem, a calcium channel blocker, is known to suppress platelet function in vitro. However, its in vivo effects on platelets have been controversial. The effect of diltiazem on both human and calf platelets was studied using impedance whole-blood aggregometry. In vitro, platelet aggregation induced by ADP (5 microM) or collagen (1 micrograms/ml) was significantly suppressed by 0.1 to 1.0 mM (45 to 450 micrograms/ml) of diltiazem in both species. In calves weighting 70 to 90 kg, platelet aggregability did not change after the oral administration of 180 mg diltiazem. In this condition, diltiazem was not detected in plasma samples. Intravenous injection of 0.5 mg/kg diltiazem also did not significantly alter the aggregability, although the PR interval on the ECG elongated (40 msec, p < .05), mean arterial pressure dropped (14 mmHg, p < .05), and diltiazem was readily detected in plasma (199 ng/ml, 0.4 microM). In conclusion, platelet aggregability is not altered by a clinical dosage of diltiazem that is sufficient to induce hemodynamic changes with therapeutic plasma concentrations.